Genital Warts

Updated: Nov 17, 2016
  • Author: Delaram Ghadishah, MD; Chief Editor: William D James, MD  more...
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Overview

Background

Genital warts are an epidermal manifestation attributed to the epidermotropic human papillomavirus (HPV). More than 100 types of double-stranded HPV papovaviruses have been isolated thus far, and, of these, about 35 types have affinity to genital sites. Many have been linked directly to an increased neoplastic risk in men and women.

Two general categories of genital human papillomavirus (HPV) exist: low-risk benign HPV lesions and high-risk neoplastic HPV lesions. The low-risk strains are responsible for genital warts and recurrent respiratory papillomatosis (RRP), as well as low-grade cervical lesions. Two types, 6 and 11, account for more than 90% of genital warts and most cases of RRP. These are least likely to have malignant potential.

Thirteen human papillomavirus (HPV) types (ie, 33, 35, 39, 40, 43, 45, 51-56, 58) have a moderate risk for neoplastic conversion; HPV-16 and HPV-18 are considered high risk; more than 70% of cervical, vaginal, and penile cancers are caused from 2 types. This picture is complicated by the proven coexistence of many types in the same patient (10-15%), lack of adequate information on the oncogenic potential of many other types, and ongoing identification of additional HPV-related clinical pathology. For example, bowenoid papulosis, seborrheic keratoses, and Buschke-Lowenstein tumors —previously parts of the differential diagnosis of genital warts—all have been linked to HPV infections.

Bowenoid papulosis consists of rough papular eruptions and is considered a carcinoma in situ. Eruptions can be red, brown, or flesh colored and may regress or become invasive.

Seborrheic keratoses previously were considered a benign skin manifestation. These consist of rough plaques and have an infectious and an oncogenic potential.

Buschke-Lowenstein tumor (giant condyloma) is a fungating, locally invasive, low-grade cancer attributed to HPV.

Also see Human Papillomavirus.

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Pathophysiology

Human papillomavirus (HPV) invades cells of the basal layer of the epidermis, penetrating skin and mucosal microabrasions in the genital area.

A latency period of 3 weeks to 9 months may ensue. Following that period, viral DNA, capsids, and particles are produced. Host cells become infected and develop the morphologic atypical koilocytosis of genital warts.

Most frequently affected are the penis, vulva, vagina, cervix, perineum, and perianal area. These mucosal lesions occasionally can be found in the oropharynx, larynx, and trachea. HPV-6 even has been reported in other uncommon areas (eg, extremities).

Multiple simultaneous lesions are common and may involve subclinical states as well as different anatomic sites. Subclinical infections have an infectious and oncogenic potential. However, most infections are transient and clear up within 2 years without intervention.

Consider the possibility of sexual abuse in pediatric cases; however, remember that infection by direct manual contact or, rarely, by indirect transmission from fomites may occur. Additionally, passage through an infected vaginal canal at birth may cause respiratory lesions in infants.

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Epidemiology

Frequency

United States

Annual incidence is 1%, and genital warts are considered the most common sexually transmitted disease (STD). A four-fold or more increase in prevalence has been reported in the last two decades; prevalence reportedly exceeds 50%. The lifetime risk of infection is 50% in sexually active individuals.

International

Reports vary on international prevalence, but available data from England, Panama, Italy, the Netherlands, and other developed and underdeveloped countries show HPV infections to be at least as common internationally as in the United States.

Sex

Both sexes are susceptible to infection. Overt disease may be more common in men (reported in 75% of cases); however, infection may be more prevalent in women.

Age

Prevalence is greatest in persons aged 17-33 years, with a peak incidence in persons aged 20-24 years.

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Prognosis

Many cases of genital warts fail to respond to treatment or recur after adequate response. The recurrence rate of cervical dysplasia in women is not altered by treatment of their sex partners.

Recurrence rates exceed 50% after 1 year and have been attributed to the following:

  • Recurrent infection from sexual contact
  • Long incubation period of HPV
  • Location of the virus in superficial skin layers away from lymphatics
  • Persistence of the virus in the surrounding skin, in the hair follicle, or in sites inadequately reached by the intervention
  • Missed or deep lesions
  • Subclinical lesions
  • Underlying immunosuppression

Mortality is secondary to malignant transformation to a carcinoma. This oncogenic potential, which is rare with HPV-6 and HPV-11 (the most commonly isolated viruses), reportedly triples the risk of genitourinary cancer among infected males.

HPV infection appears to be more common and worse in patients with various types of immunologic deficiencies. Recurrence rate, size, discomfort, and risk of oncologic progression are highest among these patients. Secondary infection is uncommon. Latent illness often becomes active during pregnancy.

Vulvar warts may interfere with parturition. Trauma then may occur, producing crusting or erythema. Acute urethral obstruction may occur in women.

Bleeding has been reported due to flat warts of the penile urethral meatus (usually associated with HPV-16) and in the large lesions that can occur during pregnancy. Lesions may lead to disfigurement.

There is an associated psychosocial burden of external lesions on the genitalia.

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Patient Education

Identify and educate persons at risk. For patient education resources, visit the Sexual Health Center. Also, see the patient education article Genital Warts.

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